The Effects of an Increased Viral Burden in Aging and Chronic Inflammation

By 2030 21% of the U.S. population will be over 65 years old. Multiple diseases associated with aging correlate with chronic inflammation. Previous studies have shown that aging results in an "immunosenescent" state characterized by an increased number of highly differentiated effector lymphocytes which, paradoxically, spontaneously secrete large amounts of pro-inflammatory mediators. Repetitive immune stimulation causes the development of these terminally differentiated lymphocytes. We hypothesize that immunosenescence is more prevalent in older individuals due to a higher lifetime prevalence of viral infections, especially those capable of establishing latency, which results in repetitive T cell stimulation due to recurrent reactivation. In this study, we collected blood plasma from older (< 65) and younger (20-40) subjects to compare the presence of plasma inflammatory markers (using bead array assays) and evidence of T immunosenescence and activation (using flow cytometry). We further sought to determine if recognized differences correlated with evidence of cytomegalovirus (CMV) infection, a chronic viral infection capable of establishing lifelong latency. We hypothesize that the immunosenescent T cell phenotype and plasma inflammatory mediators will exhibit a correlation to evidence of CMV viral burden, and the frequency of T cell activation will be higher in older adults.